Maintenance of blood pressure by the renin–angiotensin system in normal man View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1981-05

AUTHORS

G. A. MacGregor, N. D. Markandu, J. E. Roulston, J. C. Jones, J. J. Morton

ABSTRACT

The view that the renin–angiotensin–aldosterone system is a defence mechanism that maintains blood pressure only in conditions of volume depletion or sodium restriction1 has been supported by studies with saralasin2,3, a competitive inhibitor of angiotensin II, and teprotide1, an inhibitor of angiotensin converting enzyme that blocks the formation of angiotensin II. However, both saralasin and teprotide will underestimate the role of the renin–angiotensin system because: (1) they have to be given intravenously, thus inhibiting only the short-term effects of circulating angiotensin II; (2) all subjects in these studies were rested for some time before infusion1–3; and (3) saralasin is an agonist4–7 which only inhibits the action of circulating angiotensin II when its level is high. Niarchos et al.8 demonstrated a drop in blood pressure with teprotide in normal subjects on a sodium intake of 150 mmol per day, but this was partly due to one subject fainting. Therefore, none of these studies clearly shows at what stage of volume depletion the system actively maintains blood pressure. By analogy with other biological systems, a gradual increase in the importance of the renin–angiotensin system as sodium is lost is more likely than an all-or-none phenomenon. Using the recently developed oral inhibitors of angiotensin converting enzyme9–11, it is now possible to inhibit the formation of angiotensin II long-term and study human subjects during normal activity. We have now investigated the effect of one such inhibitor, captopril, in normotensive, healthy, male subjects on a normal sodium intake. Our results demonstrate that the renin–angiotensin system maintains blood pressure in these conditions and that the system is an important controller of aldosterone secretion as well as sodium excretion on a normal sodium intake. More... »

PAGES

329-331

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/291329a0

DOI

http://dx.doi.org/10.1038/291329a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1001285573

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/7015149


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